Cases reported "Silicosis"

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1/6. A silicosis patient presenting with an enlarged supraclavicular lymph node.

    A stone splitter was discovered to have an enlarged supraclavicular lymph node which showed nodules with bi-refringent crystals on histological examination. He had worked in a dusty environment for more than 10 years with ineffective respiratory protection. He gave a history of occasional cough with blood-stained sputum for 10 years for which no definite diagnosis was made. silicosis (classified as type s/s with profusion 1/1) was confirmed after his chest radiographs were reviewed. The presentation was unusual and illustrated the importance of an occupational history in clinical practice.
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2/6. gardening in greenhouses as a risk factor for silicosis.

    silicosis is a typical occupational disease, although some cases caused by non-industrial exposure have also been reported. We saw a 53-year-old male gardener with recurrent non-productive cough. A routine radiograph of the chest showed bilateral pulmonary nodules and subsequent computed tomography suggested that the infiltrates could be metastases. Open lung biopsy revealed nodules consisting of fibrotic tissue while the presence of birefringent silica particles was observed by polarised light microscopy. Mineralogical analysis of the substrata from the patient's workplace revealed an SiO(2) concentration of 31%. This case indicates that the inhalation of siliceous particles in a closed environment such as a greenhouse is a risk factor for silicosis.
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3/6. Silica and trichloroethylene-induced progressive systemic sclerosis.

    Several environmental factors and chemicals have been described as being able to induce systemic scleroderma and scleroderma-like diseases. The present work reports 2 male patients with progressive systemic sclerosis and pulmonary silicosis. Both patients had occupational histories of exposure to silica and one of them of handling trichloroethylene as a degreasing agent. The clinical and analytical findings could not be distinguished from those present in idiopathic systemic scleroderma with the exception of interstitial images with calcified hilar lymph nodes in the chest X-ray suggestive of pulmonary silicosis.
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4/6. silicosis in jade workers.

    The recent finding of cases of silicosis among jade workers in hong kong points to this disease being an occupational hazard. The source was found to be the silica flour that was added in a polishing process. Five cases are described together with the results of environmental investigation in a workplace. In three cases the disease was of early onset, rapidly progressive, and presented the features of galloping silicosis noted in other occupational exposures to silica flour. One patient had massive fibrosis and severe glomerulonephropathy, an association that has also been previously noted. One case showed evidence of active tubercular infection in addition to silicosis and two had healed lesions. Silica concentrations in the workplace during the suepect process were well above accepted threshold limit values.
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5/6. "Souvenir" casting silicosis.

    A case of silicosis in a 47-year-old worker who was employed for many years in a small souvenir casting shop is described. This work site demonstrates many unfavorable characteristics of small industries, such as lack of awareness of the need for safety measures, exposure control, protection of workers, and lack of compliance with environmental and medical-legal standards.
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6/6. quartz exposures and severe silicosis: a role for the hilar nodes.

    BACKGROUND: Two stonemasons working together in an environment with high concentrations of quartz pursued very different clinical courses; one died of rapidly progressive silicosis and the other developed hilar adenopathy and, later, early massive fibrosis. The exposures to quartz of these two men were investigated to allow comment on the pathogenesis of severe silicosis relative to concentrations of dust. methods: Estimates of exposure were based on previously taken personal dust samples, detailed lifetime occupational histories, and semiquantitative exposure modelling. RESULTS: One of the men who died had a 30 year exposure estimated to have averaged < 0.1 mg/m3, leading to hilar node fibrosis and calcification, followed by a five year exposure to about 2 mg/m3 which proved fatal. Estimates of exposure tallied with postmortem measurement of lung burden, suggesting retention of all dust deposited in the lungs over his final period of work. The younger man, working from the start of his apprenticeship alongside the older one, had a six year exposure to about 1.5 mg/m3, which caused hilar node enlargement and subsequent calcification but minimal lung involvement. CONCLUSIONS: Exposures to relatively low concentrations of quartz may be capable of causing hilar node fibrosis, impairing the clearance of any quartz inhaled subsequently. The findings support the concept that destruction of the hilar nodes by silicotic fibrosis, impairing lung clearance, has an important pathogenic role in the development of massive fibrosis, and in men subsequently exposed to very high concentrations of respirable quartz, rapidly progressive silicosis.
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